Key result
Simvastatin reduces plaque FDG uptake compared to diet alone at 3 months.
Why the study?
Inflammation plays a key role in progression and destabilization of atherosclerotic plaque, and the antiinflammatory effects of statins on plaque inflammation needed investigation.
Does simvastatin reduce atherosclerotic plaque inflammation measured by 18F-FDG PET in subjects with 18F-FDG uptake in the aorta or carotid arteries?
RCT (n=43)
randomized
Does simvastatin reduce atherosclerotic plaque inflammation measured by 18F-FDG PET in subjects with 18F-FDG uptake in the aorta or carotid arteries?
Simvastatin reduces atherosclerotic plaque inflammation assessed by 18F-FDG PET, with effects that correlate with HDL-C elevation rather than LDL-C reduction.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“Although their study yielded positive results, the magnitude of the effect would surely have been greater with a higher dose of a more powerful statin, and this might have answered some of the questions with which the researchers were left at the end of their study, such as why the FDG reduction induced by statin treatment correlated more closely with the high-density lipoprotein increase than with low-density lipoprotein decrease.”
Simvastatin attenuated plaque inflammation on FDG-PET; leaves open whether this supports broader use or improves outcomes.
OBJECTIVES: We investigated whether simvastatin attenuates plaque inflammation by using 18F-fluorodeoxyglucose positron emission tomography (18FDG-PET) co-registered with computerized tomography. BACKGROUND: Inflammation plays a key role in progression and destabilization of atherosclerotic plaque. 18F-fluorodeoxyglucose PET is a promising tool for visualizing inflammation of atherosclerotic plaque. Antiinflammatory action is one of the pleiotropic effects of statins. METHODS: Forty-three consecutive subjects, who underwent 18FDG-PET for cancer screening and had 18FDG uptakes in the thoracic aorta and/or the carotid arteries, were randomized to either statin group receiving simvastatin (n = 21) or diet group receiving dietary management only (n = 22). The maximum standardized uptake values (SUVs) were measured in individual plaques, and were averaged for analysis of the subjectwise results. The responses were assessed after 3-month treatments. RESULTS: Positron emission tomography revealed 117 and 123 18FDG-positive plaques in the statin and diet groups, respectively. Simvastatin, but not diet alone, attenuated plaque (18)FDG uptakes and decreased the SUVs (p < 0.01). Simvastatin reduced low-density lipoprotein cholesterol (LDL-C) by 30% (p < 0.01) and increased high-density lipoprotein cholesterol (HDL-C) by 15% (p < 0.01), whereas LDL-C and HDL-C levels were not changed in the diet group. In the statin group, the decrease in the SUV was well correlated with the HDL-C elevation (p < 0.01) but not with the LDL-C reduction. CONCLUSIONS: 18F-fluorodeoxyglucose PET visualized plaque inflammation and simvastatin attenuated it. The LDL-C-independent effects of simvastatin may participate in the beneficial effect. 18F-fluorodeoxyglucose PET has a potential for visually monitoring plaque inflammation and the therapeutic effectiveness of statins.
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Tahara et al. (2006) conducted an RCT in Atherosclerotic plaque inflammation (n=43). Simvastatin vs. Dietary management only was evaluated on Maximum standardized uptake values (SUVs) in individual plaques (p=<0.01). Simvastatin, but not diet alone, attenuated plaque 18FDG uptakes and decreased maximum standardized uptake values after 3 months of treatment (P<0.01).
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